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A possible target of antioxidative therapy for diabetic vascular complications-vascular NAD(P)H oxidase
T Inoguchi1, H Tsubouchi, T Etoh
1Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. toyoshi@intmed3.med.kyushu-u.ac.jp
Abstract:
A growing body of evidence has shown that oxidative stress may be involved in the development of vascular complications associated with diabetes. However, the molecular mechanism for increased reactive oxygen species (ROS) production in diabetes remains uncertain. Among various possible mechanisms, attention have increasingly been paid to NAD(P)H oxidase as the most important source of ROS production in vascular cells. High glucose level stimulates ROS production through protein kinase C (PKC)-dependent activation of vascular NAD(P)H oxidase. Furthermore, the expression of NAD(P)H oxidase components is increased in micro- and macrovascular tissues of diabetic animals in association with various functional disorders and histochemical abnormalities. These results suggest that vascular NAD(P)H oxidase-driven ROS production may contribute to the onset or development of diabetic micro- or macrovascular complications. In this point of view, the possible new strategy of antioxidative therapy for diabetic vascular complications is discussed in this review.
Insights
Diabetic vascular complications may stem from oxidative stress caused by increased reactive oxygen species (ROS) production. Targeting NAD(P)H oxidase offers a potential antioxidative therapy strategy for diabetes.
Area of Science:
- Biochemistry
- Molecular Biology
- Vascular Biology
Background:
- Oxidative stress is implicated in diabetic vascular complications.
- The precise molecular mechanisms of increased reactive oxygen species (ROS) in diabetes are not fully understood.
- NAD(P)H oxidase is increasingly recognized as a significant source of ROS in vascular cells.
Purpose of the Study:
- To review the role of NAD(P)H oxidase in diabetic vascular complications.
- To explore the molecular mechanisms of ROS production in diabetes.
- To discuss antioxidative therapy strategies targeting NAD(P)H oxidase.
Main Methods:
- Review of existing literature on oxidative stress and diabetes.
- Analysis of studies investigating NAD(P)H oxidase activity and expression in diabetic models.
- Examination of the role of protein kinase C (PKC) in high glucose-induced ROS production.
Main Results:
- High glucose stimulates ROS production via PKC-dependent activation of vascular NAD(P)H oxidase.
- Increased expression of NAD(P)H oxidase components is observed in diabetic animal vascular tissues.
- These changes correlate with functional disorders and histochemical abnormalities in diabetic vasculature.
Conclusions:
- Vascular NAD(P)H oxidase-driven ROS production likely contributes to diabetic micro- and macrovascular complications.
- Targeting NAD(P)H oxidase represents a potential therapeutic strategy for managing diabetic vascular disease.
- Further research into antioxidative therapies for diabetic complications is warranted.